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New UCLA research could help explain the link between a high-cholesterol diet and an elevated risk for colon cancer. In a study of mice, scientists from the David Geffen School of Medicine at UCLA discovered that boosting the animals’ cholesterol levels spurred intestinal stem cells to divide more quickly, enabling tumors to form 100 times faster. The study identifies a molecular pathway that could serve as a new drug target for colon cancer treatment.
Cholesterol influences the growth of stem cells in the intestines, which in turn accelerates the rate of tumor formation. The connection between dietary cholesterol and colon cancer is well established. The scientists increased cholesterol in the intestinal stem cells in some of the mice by introducing more of the substance into their diets.
In others, the researchers altered a gene that regulates phospholipids, the primary type of fat in cell membranes, which spurred the cells into producing more cholesterol on their own. The stem cells ‘ ability to multiply increased in both groups.
As the animals’ cholesterol levels rose, their cells divided more rapidly, causing the tissue lining their guts to expand and their intestines to lengthen. These changes significantly sped up the rate of tumor formation in their colons.
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